HIV-related discrimination amongst healthcare providers is one of the strongest obstacles to effectively responding to HIV. This study was conducted to explore the occurrence of and other factors related to discrimination against people living with HIV/AIDS amongst healthcare providers in Guangzhou, China. This was a cross-sectional study, conducted between July and October 2016, that enrolled healthcare providers from 9 healthcare institutions in Guangzhou, China. HIV-related discrimination was assessed using anonymous self-designed questionnaires. Chi-square tests were used to study the differences in the socio-demographic characteristics, occupational characteristics, HIV-related knowledge and personal attitudes between participants who had and had not discriminated against People living with HIV/AIDS (PLWHA). A multivariate logistic regression analysis was used to study the factors associated with HIV-related discrimination. A total of 972 healthcare providers were investigated, and 386 (39.7%) had previously served HIV-positive individuals in their work. Administering HIV antibody tests for patients without his or her consent was the most frequent act of discrimination (65.3%), and other forms of discrimination, including “differential treatment” (51.0%), “disclosed information” (46.4%) and “refused to treat” (38.6%), were also prevalent. The logistic regression analysis indicated that people who had worked for 3–7 years, worked in secondary hospitals or lower, worked in surgical departments, had lower scores on HIV transmission knowledge, were dissatisfied with the occupational exposure protection system offered by the government, were worried about HIV-related exposure and feared HIV-related exposure were more likely to commit an act of medical discrimination against PLWHA. HIV-related discrimination was not unusual in the healthcare providers of Guangzhou, which may be related to their negative cognitions and attitudes as well as the hospital management system and government policy. Therefore, comprehensive HIV-related knowledge education should be implemented to change the attitude of healthcare providers. In addition, the current laws and regulations should be refined by the government to protect the rights of healthcare providers. The contradiction between designated hospitals and non-designated hospitals should be resolved to ensure that PLWHA receive timely and effective help and treatment.

Acute T-lymphocyte leukaemia is a form of haematological malignancy with abnormal activation of NF-κB pathway, which results in high expression of A20 and ABIN1, which constitute a negative feedback mechanism for the regulation of NF-κB activation. Clinical studies have found that acute T-lymphocyte leukaemia patients are susceptible to Toxoplasma gondii infection; however, the effect of T. gondii on the proliferation and apoptosis of human leukaemia T-cells remains unclear. Here, we used the T. gondii ME-49 strain to infect human leukaemia T-cell lines Jurkat and Molt-4, to explore the effect of T. gondii on proliferation and apoptosis, which is mediated by NF-κB in human leukaemia T-cells. The Tunel assay was used to detect cell apoptosis. Cell Counting Kit-8 was used to detect cell proliferation viability. The apoptosis level and the expression level of NF-κB related proteins in human leukaemia T-cells were detected by flow cytometry and Western blotting. Western blotting analyses revealed that the T. gondii ME-49 strain increased the expression of A20 and decreased both ABIN1 expression and NF-κB p65 phosphorylation. By constructing a lentiviral-mediated shRNA to knockdown the A20 gene in Jurkat T-cells and Molt-4 T-cells, the apoptosis levels of the two cell lines decreased after T. gondii ME-49 infection, and levels of NF-κB p65 phosphorylation and ABIN1 were higher than in the non-konckdown group. After knockingdown ABIN1 gene expression by constructing the lentiviral-mediated shRNA and transfecting the recombinant expression plasmid containing the ABIN1 gene into two cell lines, apoptosis levels and cleaved caspase-8 expression increased or decreased in response to T. gondii ME-49 infection, respectively. Our data suggest that ABIN1 protects human leukaemia T-cells by allowing them to resist the apoptosis induced by T. gondii ME-49 and that the T. gondii ME-49 strain induces the apoptosis of human leukaemia T-cells via A20-mediated downregulation of ABIN1 expression.